6533b83afe1ef96bd12a7992

RESEARCH PRODUCT

Anxiolytic-like effects of acute and chronic GABA transporter inhibition in rats.

Hartmut LüddensUlrich SchmittChristoph Hiemke

subject

AgonistMalemedicine.medical_specialtyElevated plus mazeZolpidemGABA Plasma Membrane Transport ProteinsTime FactorsTiagabinemedicine.drug_classPyridinesNipecotic AcidsOrganic Anion TransportersPharmacologyAnxiolyticDrug Administration Schedulechemistry.chemical_compoundInternal medicinemedicineGABA transporterAnimalsNeurotransmitterMaze LearningTiagabineBiological PsychiatryDiazepambiologyBehavior Animalbusiness.industryMembrane ProteinsMembrane Transport ProteinsDrug SynergismRats Inbred StrainsRatsZolpidemPsychiatry and Mental healthEndocrinologyNeurologychemistryAnti-Anxiety Agentsbiology.proteinNeurology (clinical)businessCarrier ProteinsDiazepammedicine.drug

description

Acute GABA transporter inhibition can induce anxiolytic-like behaviors. The present analysis addressed whether chronic treatment (23 days via drinking water) with a GABA transporter inhibitor affects rat behavior similar to acute treatment and interferes with additional benzodiazepine-receptor agonistic treatment. Seventy-one rats divided into seven groups were acutely treated with either vehicle, diazepam (2 mg/kg), zolpidem (0.05 mg/kg), tiagabine (19 mg/kg) or chronically with tiagabine with or without acute diazepam or zolpidem. Animals were behaviorally characterized in an elevated plus-maze. None of the treatments induced changes in the activity of the animals. Acute and chronic treatment with tiagabine induced anxiolytic-like effects, similar to acute doses of diazepam. Acute diazepam did not enhance chronic tiagabine effects, whereas acute zolpidem attenuated the anxiolytic-like effects of chronic tiagabine. It is concluded that anxiolytic effects of acute GABA-uptake inhibition by tiagabine persist under chronic treatment and are sensitive to concomitant use of benzodiazepine receptor ligands.

yearjournalcountryeditionlanguage
2002-05-01Journal of neural transmission (Vienna, Austria : 1996)
10.1007/s007020200071https://pubmed.ncbi.nlm.nih.gov/12111474